Please use this identifier to cite or link to this item :http://hdl.handle.net/2066/33055

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Subject:

Cellular Animal Physiology

Organization:

Neurophysiology

Former Organization:

Cellular Animal Physiology

Journal title:

Neuroendocrinology

Volume:

vol. 81

Issue:

iss. 3

Page start:

p. 167

Page end:

p. 173

Abstract:

It is known that intracerebroventricular (ICV) administration of a low dose of interleukin-1beta (IL-1beta) induces hyperalgesia and that this effect can be inhibited by alpha-melanophore-stimulating hormone (alpha-MSH). To identify the part of the brain that is affected by hyperalgesia-induced IL-1beta and the possible site of alpha-MSH inhibition, we have examined Fos expression in the rat brain in response to ICV microinjection of alpha-MSH and/or IL-1beta. Following injection of 10 pg IL-1beta, hyperalgesia was induced and Fos became expressed in the paraventricular nucleus (PVN) of the hypothalamus and in the arcuate nucleus (ARC), which contains alpha-MSH-producing neurons. IL-1beta injection did not induce Fos expression in the pars intermedia of the pituitary gland, which contains endocrine melanotrope cells that release alpha-MSH into the systemic circulation. ICV co-injection of IL-1beta with 30 ng alpha-MSH fully inhibited both hyperalgesia and Fos expression in the PVN and the ARC. We conclude that PVN neurons are activated by hyperalgesic IL-1beta and propose that this effect is abolished by alpha-MSH possibly released from the ARC but not from the pituitary gland.